Myeloid CD11c+ antigen-presenting cells ablation prevents hypertension in response to angiotensin II plus high-salt diet

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dc.contributor.authorHevia, Daniel
dc.contributor.authorAraos, Patricio
dc.contributor.authorPrado, Carolina
dc.contributor.authorLuppichini, Eugenia Fuentes
dc.contributor.authorRojas, MacArena
dc.contributor.authorAlzamora, Rodrigo
dc.contributor.authorCifuentes-Araneda, Flavia
dc.contributor.authorGonzalez, Alexis A.
dc.contributor.authorAmador, Cristian A.
dc.contributor.authorPacheco, Rodrigo
dc.contributor.authorMichea, Luis
dc.date.accessioned2022-09-14T14:16:11Z
dc.date.available2022-09-14T14:16:11Z
dc.date.issued2018
dc.descriptionIndexación Scopuses
dc.description.abstractIncreasing evidence shows that antigen-presenting cells (APCs) are involved in the development of inflammation associated to hypertension. However, the potential role of APCs in the modulation of renal sodium transport has not been addressed. We hypothesized that APCs participate in renal sodium transport and, thus, development of high blood pressure in response to angiotensin II plus a high-salt diet. Using transgenic mice that allow the ablation of CD11chigh APCs, we studied renal sodium transport, the intrarenal renin-angiotensin system components, blood pressure, and cardiac/renal tissue damage in response to angiotensin II plus a high-salt diet. Strikingly, we found that APCs are required for the development of hypertension and that the ablation/restitution of APCs produces rapid changes in the blood pressure in mice with angiotensin II plus a high-salt diet. Moreover, APCs were necessary for the induction of intrarenal renin-angiotensin system components and affected the modulation of natriuresis and tubular sodium transporters. Consistent with the prevention of hypertension, the ablation of APCs also prevented cardiac hypertrophy and the induction of several indicators of renal and cardiac damage. Thus, our fndings indicate a prominent role of APCs as modulators of blood pressure by mechanisms including renal sodium handling, with kinetics that suggest the involvement of tubular cell functions in addition to the modulation of inflammation and adaptive immune response. © 2017 The Authors.es
dc.description.urihttps://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.117.10145
dc.identifier.citationHypertension Volume 71, Issue 4, Pages 709 - 718 2018es
dc.identifier.doi10.1161/HYPERTENSIONAHA.117.10145
dc.identifier.issn0194911X
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/23870
dc.language.isoenes
dc.publisherLippincott Williams and Wilkinses
dc.rights.licenseCC BY-NC-ND
dc.subjectAngiotensin IIes
dc.subjectRenal Hypertensiones
dc.subjectAnimalses
dc.subjectAntigen-presenting cellses
dc.subjectEpithelial sodium channeles
dc.subjectInflammationes
dc.titleMyeloid CD11c+ antigen-presenting cells ablation prevents hypertension in response to angiotensin II plus high-salt dietes
dc.typeArtículoes
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